高温,噪声及二者结合对大鼠血浆部分生化指标的影响

为探讨环境因素对飞行人员的影响，８０只Ｗｉｓｔａｒ大鼠随机分为：高温组、噪声组、两组条件相加的复合组和对照组。用特异性放射免疫法测定各组血浆心钠素（ＡＮＰ）、心脏扩张素（ＣＤＤ）、内源性洋地黄因子（ＥＤＬＳ）、血浆紧张素Ⅱ（ＡⅡ）及内皮素（ＥＴ）含量。高温组血浆ＡＮＰ含量明显低于对照组（Ｐ〈０．０５）。高温组、噪声组血浆ＣＤＤ含量明显高于对照组（Ｐ〈０．０５）。高温组、噪声组及复合组血浆ＡⅡ明显高     

急性颅脑损伤后脑脊液中心钠素、精氨酸加压素的含量变化

对３４例急性脑外伤病人脑脊液（ＣＳＦ）心钠素（ＡＮＦ）、精氨酸加压素（ＡＶＰ）的含量进行放射免疫测定。结果表明，脑外伤后４８ｈ和６～１０ｄＣＳＦ中ＡＮＦ含量均明显低于对照组（Ｐ＜０．０１）；ＡＶＰ含量较对照组明显升高（Ｐ＜０．０１）。伤后２～３周ＣＳＦ中ＡＮＦ水平升高，与对照组相比无明显差异（Ｐ＞０．０５）；ＡＶＰ水平降低，但仍明显高于对照组（Ｐ＜０．０１）。ＧＣＳ≤８分者ＣＳＦ中ＡＶＰ含量高于ＧＣＳ＞８分者（Ｐ＜０．０５）；ＣＳＦ压力≥１．９６ｋＰａ者ＡＶＰ含量高于ＣＳＦ压力＜１．９６ｋＰａ者（Ｐ＜０．０５）。ＡＮＦ的含量变化与ＧＣＳ计分和ＣＳＦ压力无关。提示，ＡＮＦ和ＡＶＰ可能参与了颅脑损伤的发病机制，ＡＮＦ的分泌减少与ＡＶＰ的释放增加可能是导致脑外伤后继发脑水肿的重要因素。动态观察ＣＳＦ中ＡＮＦ和ＡＶＰ的含量变化，对于探讨颅脑损伤后的病理机制，判断脑水肿的严重程度，指导临床治疗具有重要意义。     

实验性脑损伤后脑皮质及血浆儿茶酚胺含量的改变

采用大鼠脑损伤模型，高效液相色谱法检测伤后６、２４、７２及１６８小时脑皮质及血浆儿茶酚胺（ＣＡ）含量。结果表明，脑皮质ＣＡ含量在伤后６小时显著升高，去甲肾上腺素（ＮＥ）、肾上腺素（Ｅ）及多巴胺（ＤＡ）分别为对照组的２００％（Ｐ＜０．０１）、２９５％（Ｐ＜０．００１）和１２６％（Ｐ＜０．０５），其后迅速下降，于伤后７２小时３种ＣＡ含量均明显低于正常值（Ｐ＜０．０５）。血浆ＣＡ含量也于伤后６小时达峰值，ＮＥ、Ｅ及ＤＡ分别达对照组的３３１％（Ｐ＜０．０１），７４０％（Ｐ＜０．００１）和１８０％（Ｐ＜０．０５），以后缓慢回降，至伤后１６８小时ＮＥ、Ｅ含量仍明显高于正常值（Ｐ＜０．０５）。对脑损伤后ＣＡ变化的机理及其对继发性脑损害的影响进行了讨论。     

高原肺水肿治疗前后血浆一氧化氮和心钠素含量的变化

目的：研究高原肺水肿的发生与血浆一氧化氮（ Ｎ Ｏ） 、一氧化氮合成酶（ Ｎ Ｏ Ｓ） 和心钠素（ Ａ Ｎ Ｐ） 的关系。方法：在海拔３ ７００ｍ 对１１ 例高原肺水肿患者在治疗前和治愈后分别检测其血浆 Ｎ Ｏ、 Ｎ Ｏ Ｓ和 Ａ Ｎ Ｐ含量，并与初入海拔３ ７００ ｍ 的１０ 名健康青年作对照。结果：高原肺水肿组 Ｎ Ｏ 治愈后较治疗前增高非常显著（ Ｐ＜ ０ ．０１） ， Ａ Ｎ Ｐ 降低非常显著（ Ｐ＜ ０ ．０１） ， Ｎ Ｏ Ｓ 无显著性差异（ Ｐ＞ ０ ．０５） ；治愈后 Ｎ Ｏ 和 Ａ Ｎ Ｐ显著低于健康青年组（ Ｐ＜ ０ ．０５） ，治疗前较健康青年 Ｎ Ｏ、 Ｎ Ｏ Ｓ降低非常显著（ Ｐ＜ ０ ．０１） ， Ａ Ｎ Ｐ 增高显著（ Ｐ＜ ０ ．０５） 。治疗前血浆 Ｎ Ｏ 含量与 Ｎ Ｏ Ｓ 活性呈高度正相关（ｒ＝ ０ ．８６４６ ， Ｐ＜ ０ ．０１） 。结论：血浆 Ｎ Ｏ、 Ｎ Ｏ Ｓ和 Ａ Ｎ Ｐ均参与了高原肺水肿的病理生理过程，血浆 Ａ Ｎ Ｐ含量升高可能是机体的一种保护性代偿机制。     

白细胞介素-10和地塞米松对人外周血单个核细胞核因子-κB活化及肿瘤坏死因子产生的影响

为观察白细胞介素－１０（ＩＬ－１０）和地塞米松（Ｄｅｘ）对核因子－κＢ（ＮＦ－κＢ）的活化及α肿瘤坏死因子（ＴＮＦα）释放的影响,采用分离培养的人外周血单个核细胞（ＰＢＭＣ）,分为正常对照组、脂多糖（ＬＰＳ）刺激组、ＩＬ－１０ 和Ｄｅｘ 干预组。用凝胶电泳迁移率改变分析法（ＥＭＳＡ）检测ＰＢＭＣ核提取物中ＮＦ－κＢ的活性,ＥＬＩＳＡ法检测培养上清中ＴＮＦα的含量。结果发现,ＬＰＳ刺激后１ｈ ＮＦ－κＢ活性显著高于正常对照组（Ｐ＜ ０．０１）,ＴＮＦα的释放显著增加（Ｐ＜ ０．０１）;ＩＬ－１０、Ｄｅｘ 显著抑制ＮＦ－κＢ活性（Ｐ＜ ０．０１） ,也显著抑制ＴＮＦα的释放。提示抑制ＮＦ－κＢ激活和ＴＮＦα的产生可能是ＩＬ－１０ 和Ｄｅｘ 发挥抗炎作用的重要机制之一     

高原失血性休克及再灌注后狗的死亡原因分析

本文用放射免疫法检测了海拔３６５８ｍ（大气压６５．１７ｋＰａ，氧分压１３．５８ｋＰａ）１６条高原失血性休克狗血浆心钠素（ＡＮＰ）、内源性洋地黄因子（ＥＤＦ）、肾素活性（ＰＲＡ）、血管紧张素Ⅱ（ＡⅡ）的含量，结果：实验中死亡的６条狗其休克期血浆ＡＮＰ、ＥＤＦ浓度较１０条存活狗显著降低（Ｐ＜０．０５、Ｐ＜０．０１），而血浆ＰＲＡ，ＡⅡ水平明显升高（Ｐ均＜０．０１）。揭示上述激素的异常改变是导致狗死亡的重要原因。     

高血压病患者血浆一氧化氮,血管紧张素Ⅱ的变化及意义

目的探讨高血压病患者血浆一氧化氮（ＮＯ）、血管紧张素Ⅱ（ＡｎｇⅡ）浓度的变化及其与高血压发病关系。方法用重氮法和放射免疫法分别检测５０例ＥＨ患者治疗前后及３６例正常对照组血浆ＮＯ、ＡｎｇⅡ浓度。结果（１）ＥＨ患者血浆ＮＯ浓度较正常对照组明显降低（Ｐ＜００１）,ＡｎｇⅡ较正常对照组明显增高（Ｐ＜００１）,经降压治疗后ＥＨ患者血浆ＡｎｇⅡ浓度恢复至正常,ＮＯ浓度有明显地增高（Ｐ＜００１）,但仍明显低于正常对照组（Ｐ＜００１）;（２）ＥＨ患者血浆ＮＯ与ＡｎｇⅡ呈负相关（γ＝－０８６,Ｐ＜００１）;（３）ＥＨ患者平均动脉压（ＭＡＰ）与ＮＯ呈负相关,与ＡｎｇⅡ呈正相关（γ＝－０８２,Ｆ＝５１０３,Ｐ＜００１）。结论ＮＯ、ＡｎｇⅡ共同参与高血压的发生和发展。     

烧伤,冲击伤和烧冲复合伤对肺微血管内皮细胞损伤的比较

目的：比较烧伤、冲击伤和烧冲复合伤时肺微血管内皮细胞的损伤情况．方法：用ＥＬＩＳＡ和免疫组化结合半定量的方法检测了正常及伤后血浆血管性假血友病因子（ｖＷＦ）含量和肺微血管内皮细胞ｖＷＦ含量积分变化．结果：各致伤组伤后血浆ｖＷＦ含量均较正常对照组明显增多（Ｐ＜０．０１），复合伤组最明显；而肺微血管内皮细胞ｖＷＦ含量积分则较对照明显减少（Ｐ＜０．０１），冲击伤和复合伤组血浆ｖＷＦ增多与肺微血管ｖＷＦ含量减少呈显著负相关关系，烧伤组两指标变化相关不显著．结论：复合伤时肺微血管内皮细胞受损较单纯烧伤或冲击伤均明显加重     

创伤性腹腔内出血血液不凝机制的研究

目的 研究创伤性腹腔内出血血液不凝固的机制。方法 采用Ｃｏｕｌｔｅｒ（ＪＴ－ＩＲ），ＡＣＬ３０００ｐｌｕｓ和ＥＬＩＳＡ分别检测１５例创伤性腹腔内出血病人外周静脉血和腹腔血的血小板计数（ＰＣ）、血浆血小板α颗粒膜糖蛋白１４０（ＧＭＰ－１４０）、纤维蛋白原（Ｆｇ）和Ｄ－二聚体（Ｄ－Ｄ）含量。结果 与外周静脉血比较，腹腔血中ＰＣ和Ｆｇ明显减少（Ｐ〈０．０１）、ＧＭＰ－１４０和Ｄ－Ｄ明显升高（Ｐ〈０．０１     

缺氧对肺动脉内皮细胞和平滑肌细胞分泌血管活性肽的影响

用放射免疫测定和免疫组化法缺氧对培养的小牛肺动脉内皮细胞（ＰＡＥＣ）和肺动脉平滑肌细胞（ＰＡＳＭ）自分泌心钠素（ＡＮＰ）、血管紧张素Ⅱ（ＡＴⅡ）和内源性洋地黄因子（ＥＤＬＦ）的影响。无氧培养２４ｈ末，ＰＡＥＣ分泌ＡＮＰ减少４３．５％（Ｐ〈０．００１），ＡＴⅡ和ＥＤＬＦ呈明显负相关（ｒ为－０．８８和－０．７８６，Ｐ〈０．０１），细胞内ＡＮＰ阳性颗粒也显著减少（Ｐ〈０．００１）；ＰＡＳＭ分泌ＡＮＰ无显     

连续性血液净化治疗顽固性心力衰竭患者35例结果分析

目的 探讨连续性血液净化(CBP)治疗顽固性心力衰竭(RHF)及对血浆血管紧张素Ⅱ(AngⅡ)、醛固酮(ALD)、心钠素(ANF)水平的影响。方法 应用CBP治疗35例RHF患者,检测治疗前后血压、心率、呼吸、血氧饱和度、血生化、血气分析、左心室射血分数(LVEF)及血浆AngⅡ、ALD、ANF等指标的变化和治疗效果。结果 应用CBP治疗后患者水肿明显减轻,收缩压、舒张压下降,心率、呼吸减慢,血氧饱和度升高,血清钾、钠、氯恢复正常,尿素氮及血肌酐下降;血pH值、血碳酸氢根升高,血氧分压升高,LVEF明显增加,心功能明显改善,血浆AngⅡ、ALD、ANF显著降低,统计学有明显差异。结论 CBP能有效纠正RHF患者水、电解质、酸碱平衡紊乱,降低血浆AngⅡ、ALD、ANF水平,纠正心力衰竭,短期效果佳。     

运动心脏内分泌功能可复性的研究

为了进一步探讨运动心脏的可复性及其与病理心脏的本质差异,通过动物实验模拟运动心脏,观察了停止运动训练８周后心脏重量的变化,并对心肌组织与血浆中心钠素和降钙素基因相关肽含量进行了放射免疫测定。结果显示,经过１２周耐力训练后,心脏重量指数显著增高５１％;心房肌组织与血浆中心钠素含量分别显著增高４９％和７９％;心房肌组织与血浆中降钙素基因相关肽含量分别显著增高３６％和１９％。停止训练８周后,心脏重量指数较训练时显著降低２４％,心脏绝对重量和心脏重量指数与其对照组无显著差异;心房肌组织与血浆中心钠素含量分别较训练时显著降低２２％和３３％,基本恢复到正常对照水平;心房、心室肌组织与血浆降钙素基因相关肽含量分别较训练时降低１７％、８％和３％,也恢复到正常对照水平。研究结果表明,运动心脏确有心肌肥大,同时,运动心肌组织,尤其心房组织中心钠素和降钙素基因相关肽的产生与分泌水平增高,对运动性心肌肥大的发生、心肌收缩性的增强及冠脉循环的改善起重要调节作用。停训后运动心肌细胞心钠素和降钙素基因相关肽的改变不仅表明运动心脏内分泌功能改变具有可复性,而且,进一步证实运动心脏与病理心脏有着本质的差别。     

体外反搏治疗冠心病前后血浆心钠素水平临床分析

血浆心钠素为心脏分泌的一种多肽激素,以右心耳含量最高。其利尿机制为:(1)增加肾小球滤过率;(2)增加肾血流量,影响逆流倍增机制;(3)使乳头部集合管钠重吸收降低;(4)抑制血管加压素的释放。体外反搏提高肾动脉灌注压,增加回心血量。提高右心房压力,使心房牵张力上升,中心静脉压增高,均可刺激心房肌细胞分泌和释放心钠素。本组病人体外反搏前血浆心钠素水平平均为2.8ng/ml,反搏后为3.4ng/ml,有显著统计学差异(t<2.703 P<0.05)。病人在体外反搏治疗后表现尿量增多,心功能明显改善。     

特技飞行对心钠素、环核苷酸及血管紧张素Ⅱ的影响

用放射免疫法测定了16名飞行员复杂特技飞行前后的血浆心钠素(ANF)、环磷酸鸟苷(cGMP)、环磷酸腺苷(cAMP)以及血管紧张素II(ATII)含量,并以16名地勤人员作对照结果发现,飞行前空地勤人员血浆ANF、cGMP、cAMP及ATII含量均无明显差异(P>0.05).特技飞行后立即,飞行组血浆ANF、cGMP及cAMP明显增高,与对照组相比,差异十分显著(P<0.001),但血浆ATII水平未见明显变化(P>0.05).至特技飞行后6h,飞行组血浆ANF含量已恢复至正常(P>0.05),但cGMP及cAMP仍维持在较高水平,与对照组相比,差异仍较显著(P相似文献   

Atrial natriuretic factor increases vascular permeability

An increase in central blood volume in microgravity may result in increased plasma levels of atrial natriuretic factor (ANF). Since elevations in plasma ANF are found in clinical syndromes associated with edema, and since space motion sickness induced by microgravity is associated with an increase in central blood volume and facial edema, we determined whether ANF increases capillary permeability to plasma protein. Conscious, bilaterally nephrectomized male rats were infused with either saline, ANF + saline, or hexamethonium + saline over 2 h following bolus injections of 125I-albumin and 14C-dextran of similar molecular size. Blood pressure was monitored and serial determinations of hematocrits were made. Animals infused with 1.0 micrograms.kg-1.min-1 ANF had significantly higher hematocrits than animals infused with saline vehicle. Infusion of ANF increased the extravasation of 125I-albumin, but not 14C-dextran from the intravascular compartment. ANF also induced a depressor response in rats, but the change in blood pressure did not account for changes in capillary permeability to albumin; similar depressor responses induced by hexamethonium were not accompanied by increased extravasation of albumin from the intravascular compartment. ANF may decrease plasma volume by increasing permeability to albumin, and this effect of ANF may account for some of the signs and symptoms of space motion sickness.     

Atrial natriuretic factor during hypoxia and mild exercise

The effect of hypoxia on plasma atrial natriuretic factor (ANF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) was evaluated during 2 h of treadmill exercise at 2 km/h, 0 grade at sea level. Six male subjects exercised on 2 separate days during normoxia (21% O2) and hypoxia (13.3 +/- 0.3% O2). No significant changes in ANF or PRA occurred during either normoxic or hypoxic exercise. However, PAC fell significantly during normoxic exercise (17.5 +/- 3.6 vs. 12.7 +/- 2.6 ng/dl, p less than 0.05) but not during hypoxic exercise. Serum potassium concentration fell during hypoxic exercise (5.0 +/- 0.1 vs. 4.4 +/- 0.1 mmol/l, p less than 0.05) along with bicarbonate (27.8 +/- 0.7 vs. 25.8 +/- 0.6 mmol/l, p less than 0.01). Between normoxic and hypoxic studies there was a significantly higher heart rate during hypoxic exercise (78 +/- 5 vs. 90 +/- 6 b/min, p less than 0.01). The major conclusion of this study is that hypoxia resulting in arterial oxygen saturations of 81 +/- 0.7% does not affect plasma atrial natriuretic factor levels during mild exercise in normal male subjects.     

Results of a 4-week head-down tilt with and without LBNP countermeasure: I. Volume regulating hormones.

The volume regulating hormones were studied during a 4-week head-down tilt (CNES HDT) in five subjects with and without (controls) lower body negative pressure (LBNP). LBNP was applied 3 times a day for 3 weeks, 4 times a day for 4 d, and 6 times a day for 3 d the last week. In both groups we observed a significant decrease in body weight (3% in controls, 0.8% in LBNP), a significant increase in plasma renin activity and aldosterone (with an amplification of their rhythms), and a significant decrease in norepinephrine with no difference between the two groups. The only major hormonal difference was observed for atrial natriuretic factor (ANF), which decreased significantly in the control group and increased in the LBNP group. These results are compared with the improvement in orthostatic tolerance (OT) after HDT in the LBNP group in the same protocol (17). We conclude that many factors could be involved in the improvement of OT. The results suggest that better conservation of plasma volume in the LBNP group might have prevented a decrease in ANF. Whether ANF plays a role in the regulation of baroreceptor reflex with an improvement in OT is currently unknown.     

加压素和心钠素在结核性、新型隐球菌性脑膜炎患者低钠血症形成中的作用

选择经临床和病原学证实的结核性脑膜炎（结脑）８例，新型隐球菌脑膜炎（隐脑）７例。观察入院时、住院第１０、２０、３０和４０ｄ时血钠、颅内压及血浆和脑脊液（ＣＳＦ）中精氨酸加压素（ＡＶＰ）、心钠素（ＡＮＦ）含量的变化。结果表明，结脑和隐脑患者血浆和ＣＳＦ中ＡＶＰ含量显著高于对照组，隐脑患者血浆ＡＮＦ含量却明显低于对照组。且血钠浓度的变化与自身颅内压的变化趋势相反。血浆ＡＶＰ含量与血钠浓度之间呈显著负相关；血浆ＡＮＦ含量与血钠亦有明显相关性。ＣＳＦＡＶＰ含量与颅内压之间呈明显正相关。提示结脑和隐脑患者低钠血症及低钢性脑水肿的形成可能与体内ＡＶＰ和ＡＮＦ分泌异常，特别是中枢ＡＶＰ含量的异常增高有关。     

Effects of hypoxemia at sea level and high altitude on sodium excretion and hormonal levels.

Acute hypoxemia at sea level is associated with decreased aldosterone secretion. This inhibition is thought to be mediated through secretion of atrial natriuretic factor (ANF). The interaction of these two hormones should result in enhanced renal salt excretion during hypoxemic conditions. This hypothesis was tested by administration of a standardized salt load to seven normal subjects during normoxemia at sea level (SL), acute hypoxemia (AH) at sea level, and high altitude (HA) (3,000 m). Urine and venous blood samples were collected and analyzed. A natriuresis and diuresis was observed only under AH conditions. It was accompanied by a decrease in plasma aldosterone levels, but did not correlate with changes in plasma aldosterone levels, ANF, or other hormones. Increased plasma renin activity (PRA) and increased norepinephrine levels were encountered at HA, suggesting sympathetic nervous system activation. No change in anti-diuretic hormone (ADH) levels with increased plasma osmolality was seen at HA. We conclude that excretion of a salt load during normobaric hypoxemia is enhanced by a decrease in plasma aldosterone levels, unrelated to changes in ANF or other hormones. The differences observed in norepinephrine, PRA, and ADH levels during HA versus AH conditions suggest that hypobaria or chronic hypoxemia may influence these hormonal responses.